Assessing Conductivity In The Cortical-Spinal Pathway Using Motor Evoked Potentials In Multiple Sclerosis And Neuromyelitis Optica Patients

OBJECTIVE: To examine the validity of using MEP to measure neurophysiologic function of central motor conduction time in MS and NMO patients. BACKGROUND: Multiple sclerosis (MS) could affect conduction speed by focal demyelination along the pathway and/or diffuse damage throughout the normal appearing white matter. Transcranial magnetic stimulation allows measurement of centrally evoked motor evoked potentials (MEPs), which provide sensitive, reproducible measures of central motor conduction time. Neuromyelitis optica (NMO) is associated with more severe focal damage, but perhaps, less diffuse brain dysfunction as compared to MS. Thus, MEPs may both provide quantitative measures of central motor conductivity, and also distinguish NMO from MS. DESIGN/METHODS: Age and gender matched MS and NMO patients were recruited at a single center (UBC Hospital MS and NMO clinic). MEPs were assessed in a single session; MRIs were also completed and used to guide TMS application via a stereotaxic system. MEPs were analyzed for onset latency, maximal peak-to-peak amplitude, and the difference between latency and peripheral conduction time. RESULTS: To date, data has been collected and analyzed from 4 NMO and 5 MS subjects. The NMO group exhibited longer average latency (26.2 SD 5.71 versus 22.8 SD 7.02 milliseconds) and reduced MEP amplitudes (270 SD 211 versus 457 SD 404 microvolts) compared to MS. CONCLUSIONS: These preliminary data suggest that individuals with NMO demonstrate less cortical excitability (as measured by onset latency and MEP amplitudes) as compared to individuals with MS. Further, they indicate that TMS based measures may be sensitive to differences in neuroelectrophysiology between individuals with NMO and MS. Future work will consider the relationship between MEP response and MRI myelin water fraction to further support the use of MEPs as a reliable tool in the assessment of functional abnormalities in MS and NMO patients. Disclosure: Dr. Manogaran has nothing to disclose. Dr. Borich has nothing to disclose. Dr. Vavasour has nothing to disclose. Dr. Zakeri has nothing to disclose. Dr. Kim has nothing to disclose. Dr. Kuan has nothing to disclose. Dr. Kolind has nothing to disclose. Dr. Boyd has nothing to disclose. Dr. McKay has nothing to disclose. Dr. Li has received personal compensation for activities with Genzyme, Novartis, and Nuron as a consultant. Dr. Li has receved research support from Angiotech, Bayer, Berlex-Schering, Bio-MS, Boehringer-Ingelheim, Centocor, Daiichi Sankyo, Genentech, Hoffmann-LaRoche, Merck-Serono, Perceptives, Schering-Plough, Teva Neurosciences, and Sanofi-Aventis. Dr. Traboulsee has received personal compensation for activities with Roche Diagnostics Corporation, EMD Serono, Teva Neuroscience, and Biogen Idec. Dr. Traboulsee has received research support from Bayer Pharmaceuticals and Roche Pharmaceuticals.